Recent studies have revealed that approximately 10 million women in the United States between the ages of 50 and 74 reported a lack of lubrication on 229 million sexual intercourse occasions. In fact, it was found that over fifty-eight percent of 260 females surveyed were affected by sexual dysfunction, as defined as pain or discomfort during sexual intercourse, diminished vaginal lubrication, delayed vaginal engorgement, increased time for arousal, diminished ability to reach orgasm, or diminished clitoral sensation.
An animal model of this syndrome was developed by Goldstein and Berman (Int. J. Impot. Res. 10 Suppl. 2:S84-90; S98-101, 1998, the disclosure of which is incorporated herein by reference). These investigators undertook diagnostic studies assessing the hemodynamic integrity of the ilio-hypogastric-pudendal arterial bed to the vagina and clitoris and new oral/topical pharmacologic strategies for enhancing vaginal/clitoral blood flow in patients with vasculogenic female sexual dysfunction. They observed that there was a growing body of evidence that women with sexual dysfunction would commonly have physiologic abnormalities, such as vasculogenic female sexual dysfunction, contributing to their overall sexual health problems.
Park et al. (Int. J. Impot. Res. 9:27-37, 1997, the disclosure of which is incorporated herein by reference) have shown that female sexual dysfunction may be related in part to vasulogenic impairment of the hypogastric-vaginal/clitoral arterial bed. In order to investigate this theory under a controlled experimental situation, they developed an animal model of vaginal engorgement insufficiency and clitoral erectile insufficiency. They achieved pelvic nerve stimulated vaginal engorgement and clitoral erection in control normal diet New Zealand White female rabbits and atherosclerotic balloon injury of aorto-iliac arteries and 0.5% cholesterol diet New Zealand White female rabbits. After 16 weeks, novel hemodynamic variables, including vaginal wall and clitoral blood flow, vaginal wall and clitoral intracavemosal pressure, vaginal length, vaginal luminal pressure, blood levels of cholesterol and triglycerides, aorto-iliac angiography and vaginal wall and clitoral erectile tissue histology, were recorded in the two groups of rabbits. Their results indicate that pelvic nerve stimulation induced vaginal hemodynamic changes, and there was significantly less increase in blood flow, wall pressure and length changes in atherosclerotic rabbits compared to the control rabbits. Histologic examination of clitoral erectile tissue demonstrated cavernosal artery atherosclerotic changes and diffuse vaginal and clitoral fibrosis. Aorto-iliac angiography in atherosclerotic animals revealed diffuse moderate to severe atherosclerotic occlusion. They conclude that vaginal engorgement and clitoral erection depend increased blood inflow.
Present day management of women with sexual arousal disorder, especially those with diminished vaginal lubrication and painful penetration is based on psychologic, hormonal and "artificial lubricant" interventions. The pathophysiology of vaginal engorgement insufficient may be, in part, related to vascular impairment.
Prostanoid compounds, such as prostaglandin E-1 (PGE-1), have been used as an adjunct to improving blood flow in arterial angioplasty procedures. See See et al., Advances in Prostaglandin, Thromboxane and Leukotriene Res., 17:266-70, 1987; See et al., Applied Cardiopulmonary Pathophysiology 2:193-98, 1998, the disclosures of which are incorporated herein by reference. Prostanoid compounds have also been used in the treatment of male erectile dysfunction. For example, U.S. Pat. No. 5,718,917, the disclosure of which is incorporated herein by reference, discloses a method for treating erectile dysfunction comprising administering prostaglandin-containing liposomes to the penis.